以傳統中藥益母草萃取物治療逼尿肌功能低下之SD大鼠的效益

楊浩誌、劉昱良、黃國財、林健煇、林威宇、陳志碩、黃雲慶、何東儒

財團法人嘉義長庚紀念醫院 外科部 泌尿科

The Efficiency of Traditional Chinese Medicine, Leonurus artemisia, for Detrusor Underactivity Treatment in Sprague-Dawley Rats models

Hao-Chih Yang, Yu-Liang Liu, Kuo-Tsai Huang, Jian-Hui Lin, Wei-Yu Lin, Chih-Shou Chen, Yun-Ching Huang, Dong-Ru Ho

Division of Urology, Department of Surgery, Chang Gung Memorial Hospital, Chiayi, Taiwan

Introduction:

  Detrusor underactivity (DU) is a prevalent condition in the aging population, characterized by

impaired bladder contractility.

  Previous studies have revealed that Leonurus artemisia (LaE), a traditional Chinese herb,

possesses cardioprotective properties, particularly in ischemic conditions. Given the similarities

between ischemic bladder dysfunction and myocardial ischemia, this study aimed to investigate

the potential of LaE, specifically its active compound leonurine, in modulating detrusor function

and reversing DU.

Materials and Methods:

  In this study, we utilized Sprague-Dawley (SD) rats as a model for DU induced by partial ligation

of the left iliac artery, simulating ischemic damage.

We checked LaE’s effect on bladder in the in vivo animal model. Female SD rats were divided

into four groups, including the control group, DU group, DU with LaE treatment, and DU with

LaE and antimuscarinic treatment.

  Urodynamic studies (UDS) were performed before and after the treatment. Bladder section was

checked with H&E stain and further trichrome stain for fibrosis evaluation affected in the DU

model.

Results:

  Our experiments demonstrated that leonurine, an active compound in Leonurus japonicus, significantly reduced fibrosis and promoted smooth muscle regeneration in an ischemia-induced detrusor underactivity model. Urodynamic studies showed improved bladder capacity and contractility in leonurine-treated groups. Histological analysis confirmed a decrease in collagen accumulation and smooth muscle degradation, major factors contributing to detrusor underactivity in ischemic conditions.

  Additional analysis on the smooth muscle cell line SV-HUC-1 revealed that leonurine impacts epithelial-mesenchymal transition (EMT) markers, suggesting a regulatory effect on cellular behavior under ischemic stress. Specifically, as shown in Western blot analysis, treatment with leonurine at varying concentrations (15, 25, and 30 µg/µl) resulted in a decrease in vimentin expression and an increase in E-cadherin expression. This indicates a shift towards maintaining epithelial integrity and reducing EMT, which may contribute to the preservation of structural and functional characteristics of the bladder smooth muscle under ischemic conditions.

Conclusion:

  Leonurine demonstrated protective and regenerative effects in an ischemia-induced DU model, highlighting its potential as a novel therapeutic agent for DU and related bladder disorders. Further studies are warranted to explore leonurine’s clinical applications.